Background: Obesity has been identified as an independent risk factor for cholelithiasis. As a treatment for obesity, bariatric surgery may increase the incidence of cholelithiasis. The risk factors for cholelithiasis after bariatric surgery remain uncertain. The purpose of this study was to explore the risk factors for postoperative cholelithiasis after weight-loss surgery and propose suggestions for clinical decision making. Methods: Four databases, PubMed, EMBASE, Web of Science and Cochrane, were systematically searched for all reports about cholelithiasis after bariatric surgery, and literature screening was performed following prespecified inclusion criteria. The included studies were all evaluated for quality according to the NOS scale. Data extraction was followed by analysis using Reviewer Manager 5.4 and StataSE 15. Results: A total of 19 articles were included in this meta-analysis, and all studies were of high quality. A total of 20,553 patients were included in this study. Sex [OR = 0.62, 95% CI (0.55, 0.71), P < 0.00001] and race [OR = 1.62, 95% CI (1.19, 2.19), P = 0.002] were risk factors for cholelithiasis after bariatric surgery. Surgical procedure, preoperative BMI, weight-loss ratio, smoking, hypertension, diabetes mellitus, and dyslipidemia were neither protective nor risk factors for cholelithiasis after bariatric surgery. Conclusion: Caucasian race and female sex are risk factors for developing cholelithiasis after bariatric surgery; surgical procedure, BMI, weight loss ratio, hypertension, diabetes mellitus, dyslipidemia, and smoking are not risk factors for cholelithiasis after bariatric surgery.

Background: Type 2 diabetes (T2D) onset is a complex, organized biological process with multilevel regulation, and its physiopathological mechanisms are yet to be elucidated. This study aims to find out the key drivers and pathways involved in the pathogenesis of T2D through multi-omics analysis. Methods: The datasets used in the experiments comprise three groups: (1) genomic (2) transcriptomic, and (3) epigenomic categories. Then, a series of bioinformatics technologies including Marker set enrichment analysis (MSEA), weighted key driver analysis (wKDA) was performed to identify key drivers. The hub genes were further verified by the Receiver Operator Characteristic (ROC) Curve analysis, proteomic analysis, and Real-time quantitative polymerase chain reaction (RT-qPCR). The multi-omics network was applied to the Pharmomics pipeline in Mergeomics to identify drug candidates for T2D treatment. Then, we used the drug-gene interaction network to conduct network pharmacological analysis. Besides, molecular docking was performed using AutoDock/Vina, a computational docking program. Results: Module-gene interaction network was constructed using MSEA, which revealed a significant enrichment of immune-related activities and glucose metabolism. Top 10 key drivers (PSMB9, COL1A1, COL4A1, HLA-DQB1, COL3A1, IRF7, COL5A1, CD74, HLA-DQA1, and HLA-DRB1) were selected by wKDA analysis. Among these, COL5A1, IRF7, CD74, and HLA-DRB1 were verified to have the capability to diagnose T2D, and expression levels of PSMB9 and CD74 had significantly higher in T2D patients. We further predict the co-expression network and transcription factor (TF) binding specificity of the key driver. Besides, based on module interaction networks and key driver networks, 17 compounds are considered to possess T2D-control potential, such as sunitinib. Conclusions: We identified signature genes, biomolecular processes, and pathways using multi-omics networks. Moreover, our computational network analysis revealed potential novel strategies for pharmacologic interventions of T2D.

Background: Obesity is associated with a significant predisposition towards cardiovascular events and acts as an important risk factor for mortality. Herein, we conducted a comprehensive meta-analysis to estimate the protective effect of bariatric surgery on disease-specific mortality and major adverse cardiovascular events (MACEs) in patients with severe obesity. Methods: PubMed and Embase were searched from inception to 4 June 2022. Eligible studies were age, sex, and BMI-matched cohort studies. The protocol for this meta-analysis was registered on PROSPERO (ID: CRD42022337319). Results: Forty matched cohort studies were identified. Bariatric surgery was associated with a lower risk of disease-specific mortality including cancer mortality [hazard ratio with 95% confidence interval: 0.46 (0.37–0.58)], cardiovascular mortality [0.38 (0.29–0.50)], and diabetes mortality [0.25 (0.11–0.57)]. Bariatric surgery was associated with a lower incidence of MACEs [0.58 (0.51–0.66)] and its components including all-cause mortality [0.52 (0.47–0.58)], atrial fibrillation [0.79 (0.68–0.92)], heart failure [0.52 (0.42–0.65)], myocardial infarction [0.55 (0.41–0.74)], and stroke [0.75 (0.63–0.89)]. According to subgroup analysis on all-cause mortality, patients with severe obesity and type 2 diabetes benefited more from bariatric surgery than those with severe obesity only (heterogeneity between groups: P=0.001), while different surgical approaches brought similar benefits (heterogeneity between groups: P=0.87). Conclusions: This meta-analysis of 40 matched cohort studies supports that bariatric surgery reduces disease-specific mortality and incidence of both MACEs and its components in patients with severe obesity compared with nonsurgical subjects. Bariatric surgery deserves a more aggressive consideration in the management of severe obesity.

Background: Effect of bariatric surgery on mobilization of site-specific body adipose depots is not well investigated. Herein, the authors conducted a prospective cohort study to assess whether bariatric surgery can differentially affect specific fat storage pools and to further investigate correlations between site-specific fat mobilization and clinical outcomes. Materials and methods: In this single-centre prospective cohort study, 49 participants underwent laparoscopic sleeve gastrectomy (LSG) from 24 May 2022 to 20 October 2022 and underwent MRI to estimate subcutaneous fat area, visceral fat area (VFA), hepatic and pancreatic proton density fat fraction (PDFF) at baseline and 3 months after surgery. The protocol for this study was registered on clinicaltrials.gov. Results: Among 49 patients who met all inclusion criteria, the median [interquartile range (IQR)] age was 31.0 (23.0–37.0) years, the median (IQR) BMI was 38.1 (33.7–42.2) kg/m² and 36.7% were male. Median (IQR) percentage hepatic PDFF loss was the greatest after bariatric surgery at 68.8% (47.3–79.7%), followed by percentage pancreatic PDFF loss at 51.2% (37.0–62.1%), percentage VFA loss at 36.0% (30.0–42.4%), and percentage subcutaneous fat area loss at 22.7% (17.2–32.4%) (P<0.001). By calculating Pearson correlation coefficient and partial correlation coefficient, the positive correlations were confirmed between change in VFA and change in glycated haemoglobin (r=0.394, P=0.028; partial r=0.428, P=0.042) and between change in hepatic PDFF and change in homoeostatic model assessment of insulin resistance (r=0.385, P=0.025; partial r=0.403, P=0.046). Conclusions: LSG preferentially mobilized hepatic fat, followed by pancreatic fat and visceral adipose tissue, while subcutaneous adipose tissue was mobilized to the least extent. Reduction in visceral adipose tissue and hepatic fat is independently associated with the improvement of glucose metabolism after LSG.